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The influence of metastatic site on the expression of CEA and cellular localization of β‐catenin in colorectal cancer
Author(s) -
Rao U Subrahmanyeswara,
Hoerster Nicole S,
Thirumala Seshadri,
Rao Prema S
Publication year - 2013
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12083
Subject(s) - medicine , colorectal cancer , cancer research , oncology , catenin , cancer , beta catenin , wnt signaling pathway , signal transduction , microbiology and biotechnology , biology
Background and Aim The usefulness of carcinoembryonic antigen ( CEA ) in the diagnosis and prognosis of colorectal cancer ( CRC ) is unclear. The aim was to analyze changes in the expression of CEA during CRC progression and metastasis, so as to determine the influence of tumor metastatic organ on the CEA expression by CRC cells. Methods The human biopsies of adenocarcinomas in colon and CRC liver and lung metastases were analyzed by immunohistochemistry for the expression of CEA . Expression of E ‐cadherin and β‐catenin was also analyzed to localize the CRC neoplastic glands in metastatic tissues. Results The CRC neoplastic glands in colon and liver expressed significantly higher amount of CEA compared with crypts in normal colon. In contrast, CRC neoplastic glands formed in lung expressed low CEA level. However, CEA expression was high in areas of tumor necrosis in lung. E ‐cadherin and β‐catenin were cell membrane‐bound in normal crypts and CRC neoplastic glands in colon and liver. Although these two proteins were also cell membrane‐bound in a majority of CRC neoplastic glands in lungs, a significant proportion of these expressed β‐catenin in the nucleus, which lacked either E ‐cadherin or β‐catenin at the cell membrane. Conclusion Our findings indicate that lung microenvironment is unique in that it suppresses the expression of CEA by CRC cells forming neoplastic glands. In addition, lung microenvironment promotes nuclear localization of β‐catenin, suggesting that the W nt signaling pathway is relatively active highly in CRC metastasized to lung, when compared with liver or colon.